Evidence map›Paper›PMID 25795788›Full record

ReviewJournal of immunology (Baltimore, Md. : 1950)2015

The role of PTPN22 risk variant in the development of autoimmunity: finding common ground between mouse and human.

David J Rawlings, Xuezhi Dai, Jane H Buckner

Abstract readReview
In one paragraph

Review in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. eLife · 2023
    Article
  4. Article
  5. Article
  6. B Cell Aberrance in Lupus: the Ringleader and the Solution.Clinical reviews in allergy & immunology · 2022
    Review
  7. Systemic lupus erythematosus as a genetic disease.Clinical immunology (Orlando, Fla.) · 2022
    Article
  8. Review
  9. Association of the single nucleotide polymorphism C1858T of theInternational journal of reproductive biomedicine · 2021
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Genetic aspects of type 1 diabetes.Annals of pediatric endocrinology & metabolism · 2019
    Article
  17. Review
  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

David J RawlingsDepartment of Pediatrics, University of Washington School of Medicine, Seattle, WA 98195; Department of Immunology, University of Washington School of Medicine, Seattle, WA 98195; Seattle Children's Research Institute, Seattle, WA 98101; and jbuckner@benaroyaresearch.org drawling@u.washington.edu.
Xuezhi DaiDepartment of Pediatrics, University of Washington School of Medicine, Seattle, WA 98195; Seattle Children's Research Institute, Seattle, WA 98101; and.
Jane H BucknerTranslational Research Program, Benaroya Research Institute, Seattle, WA 98101 jbuckner@benaroyaresearch.org drawling@u.washington.edu.

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Tomas Vaisar · 1986 to 2026
$41.4M
Defining the functional impact of T1D genes in mouse and man: a unified strategyDP3DK097672 · NIDDK · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI BUCKNER, JANE HOYT · 2012 to 2013
$4.4M
Impact of the autoimmunity associated PTPN22 1858TR01AI083455 · NIAID · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI BUCKNER, JANE HOYT · 2011 to 2014
$1.7M
Impact of the autoimmunity associated PTPN22 1858TR56AI083455 · NIAID · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI BUCKNER, JANE HOYT · 2010 to 2010
$455k
NIAID NIH HHS 5R01AI083455-04NIAID NIH HHS R01 AI083455NIAID NIH HHS R56 AI083455NIDDK NIH HHS 1DP3DK097672NIDDK NIH HHS DP3 DK097672NIDDK NIH HHS P30 DK017047
6 · The paper itself

Abstract

The PTPN22 1858T variant was among the first single nucleotide polymorphisms to be associated with multiple autoimmune diseases. Lymphocyte tyrosine phosphatase, a coding variant within the tyrosine phosphatases, is known to participate in AgR signaling; the impact of this variant on the immune response and its role in the development of autoimmunity have been a focus of study. These studies used a series of approaches, including transfected cell lines, animal models, and primary human lymphocytes, and identified multiple alterations in cell signaling and function linked to the PTPN22 variant. Conflicting findings led to questions of how best to study the role of this variant in human autoimmunity. In this review, we discuss these differences and the factors that may account for them, as well as show how an integrated approach can lead to a more complete understanding of the mechanisms that promote autoimmunity in the context of the PTPN22 1858T risk variant.

Indexed as

Genetic VariationAnimalsAutoimmune DiseasesAutoimmunityDisease Models, AnimalGenetic Association StudiesGenetic Predisposition to DiseaseHumansMicePolymorphism, Single NucleotideProtein Tyrosine Phosphatase, Non-Receptor Type 22RiskProtein Tyrosine Phosphatase, Non-Receptor Type 22

Identifiers

PMID25795788
PMCPMC4369788

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.